Search

GB virus C (GBV-C), a pan-lymphotropic flavivirus capable of persistent infection, is associated with prolonged survival and reduced T-cell activation in HIV-infected patients. GBV-C was associated with reduced CD56brt/CD16- natural killer cell and monocyte activation, and a trend toward reduced B-cell activation by measuring cell surface activation markers or HIV entry coreceptors. The GBV-C association was independent of HIV viral load. Thus, GBV-C may influence non-T-cell immune activation in individuals with HIV infection.

Background: Aplastic anemia (AA) is a serious and rare disorder characterized by a hypocellular bone marrow. Hepatitis associated aplastic anemia (HAAA) is a variant of aplastic anemia in which aplastic anemia follows an acute attack of hepatitis. Several reports have noted an association between HGV and hepatitis-associated aplastic anemia besides other hepatitis causing viruses., Case Presentation: A female girl of age 11 year with a history of loose motion for one month, vomiting for last 15 days and poor oral intake for last few days is reported here. The physical examination presents fever, pallor whereas bleeding, hepatomegaly, Splenomegaly and bruising were absent, abdominal ultrasonography confirmed the absence of hepatomegaly, Splenomegaly and lymphodenopathy. The laboratory investigation parameters were: haemoglobin 6.2 g/L, total leucocytes count 1.51, neutrophils 0.47%, absolute reticulocyte count 0.5%, Monocytes 0.16%, red cell count 3.2 mil/uL, Picked cell volume (PCV) 30.13%, Mean Corpuscular Volume (MCV) 78 fL, Mean Corpuscular Hemoglobin (MCH) 26.3 pg. The liver enzymes were alanine aminotransferease (ALT) 98 IU/L, aspartate aminotransferase (AST) 114 IU/L. Serologic and molecular tests for hepatitis A, B, C, D, E, TTV, B19 were negative, whereas HGV RNA PCR test was found positive for hepatitis G virus. The bone marrow aspirate and trephine biopsy examination revealed hypo- cellularity, erythropoiesis, myelopoiesis and megakaryopoiesis., Conclusion: HAAA is an uncommon but severe condition, which may occur following idiopathic cases of acute hepatitis. Our finding suggests the involvement of HGV in the development of aplastic anemia. In patients presenting with pancytopenia after an episode of acute hepatitis, the definitive diagnosis should be considered and confirmed by RT-PCR and if possible by bone marrow biopsy.

As little is known about liver histology in the co-infection of hepatitis C virus (HCV) and hepatitis G virus (HGV), HGV RNA was investigated in 46 blood donors with hepatitis C, 22 of them with liver biopsy: co-infection HCV / HGV (n = 6) and HCV isolated infection (n = 16). Besides staging and grading of inflammation at portal, peri-portal and lobular areas (Brazilian Consensus), the fibrosis progression index was also calculated. All patients had no symptoms or signs of liver disease and prevalence of HGV / HCV co-infection was 15.2%. Most patients had mild liver disease and fibrosis progression index, calculated only in patients with known duration of infection, was 0.110 for co-infection and 0.130 for isolated HCV infection, characterizing these patients as "slow fibrosers". No statistical differences could be found between the groups, although a lesser degree of inflammation was always present in co-infection. In conclusion co-infection HCV / HGV does not induce a more aggressive liver disease, supporting the hypothesis that HGV is not pathogenic.

Objective: To observe the long-term effect of hepatitis G virus (HGV) coinfection on hepatic pathological changes of patients with chronic hepatitis B (CHB) and explore the pathogenicity of HGV., Methods: Menghini method liver biopsy was performed on 45 patients with CHB twice with an interval of 5 years on a voluntary basis. The liver tissue of 21 cases was HGV nonstructural region 5 (HGV NS5) antigen positive by peroxidase anti-peroxidase (PAP) immunohistochemical staining assay (HGV coinfection group) in these two tests, and 24 cases were negative (HGV noncoinfection group). There was no significant difference in age, sex, course of disease, amount of serum HBV-DNA by competitive quantitative polymerase chain reaction assay and severity of hepatic pathological leisions between these two groups (P < 0.05) and they were treated with the same scheme and without sustained curative effeect. The hepatic pathological changes of the two groups after 5 years were compared and analysed retrospectively., Results: There was no significant difference in basic hepatic pathological change, severity of inflammatory activity grade and fibrosis stage in these two groups. The numbers of cases of inflammatory activity grade G1, G2, G3, and G4 were 3, 7, 7, and 4 in HGV coinfection group, and 5, 8, 7, and 4 in HGV noncoinfection group in the beginning of observation; and were 3, 5, 7, and 6 in HGV coinfection group, and 4, 6, 8, and 6 in HGV noncoinfection group after 5 years. The numbers of cases in fibrosis stages S1, S2, S3, and S4 were 4, 7, 7, and 3 in HGV coinfection group, and 6, 8, 6, and 4 HGV noncoinfection group in the beginning of observation; and were 3, 6, 5, 7 in HGV coinfection group, and 4, 7, 5, and 8 in HGV noncoinfection group after 5 years (P > 0.05)., Conclusion: HGV coinfection does not lead to the activation of hepatic pathological changes and does not speed up the progression of fibrosis in patients with CHB. HGV coinfection does not play an obvious role in long-term hepatic pathological changes of patients with CHB. HGV has at most a mild hepatic pathogenicity.

Aim: To study the pathogenicity of hepatitis G virus (HGV) and observe the genesis and pathological process of hepatitis G., Methods: HGV-RNA in serum was detected by RT-PCR assay. The immunohistochemical assays of liver tissue were performed with HGV monocoloned antibody (McAb) expressed from the region of HGV NS5 nucleic acid sequence. The clinical and pathological data of 52 patients with hepatitis G were discussed. In animal experiment, the Chinese Rhesus monkeys were infected with the serum of a patient with HGV infection. And the dynamic changes in serology and liver histology of animals were observed., Results: One hundred and fifty-four patients with HGV-RNA positive were selected from 1552 patients with various kinds of hepatitis. Of 154 patients with HGV infection, 52 were infected with HGV only, which accounted for 33.8 (52/154) and 102 with positive HGV-RNA were super-infected with other hepatitis viruses, which accounted for 66.2 (102/154). The clinical and pathological observation showed that the acute and chronic hepatitis could be induced by HGV. The slight abnormality of transaminases ALT and AST in serum of monkeys lasted nearly 12 months and histological results showed a series of pathological changes., Conclusion: HGV is a hepatotropic virus and has pathogenicty.

Objective: To elucidate the pathogenicity of GBV-C/HGV in causing viral hepatitis., Methods: The sera and bioptic liver tissues, which involved 8 cases of the second liver puncture with an interval of 2 years, from 24 cases of single GBV-C/HGV RNA positive patients were observed for more than 2 years. GBV-C/HGV RNA in the sera and liver tissues was detected by using RT-PCR and in situ hybridization, respectively. Under light and electron microscope, the pathology of the liver tissues was observed., Results: At the beginning of the observation, the mean serum alanine transaminase(ALT) level was 60.17 IU/ml(range, 42.00-87.00 IU/ml), and the positive rates of anti-E2 antibody and GBV-C/HGV RNA in the sera and NS3 and/or NS5 in the liver tissues were 4.17%, 75.00% and 54.17%, respectively. In all the examined specimens, 79.17% of them showed mild acute or chronic hepatitis, mainly presenting with degeneration of hepatocytes, mild portal inflammation. GBV-C/HGV RNA and its NS3 and/or NS5 antigens were mainly detected in hepatocytes and a few mononuclear cells. In contrast, after more than 2 years, the natural change rate (negative rate of GBV-C/HGV) of 24 cases was 66.67% (P < 0.001). 75.00% had normal ALT level (P < 0.001) and 41.67% of anti-E2 antibody in the patients was positive (P < 0.001). Through histological observation, besides 2 cases of liver tissues showing very mild hydropic degeneration, there were no abnormal findings in 8 cases of the second liver biopsy., Conclusion: GBV-C/HGV could induce mild and self-limited hepatitis, which showed that GBV-C/HGV may be a light and self-limited pathogenic agent to human liver. E2 antibody appearance may indicate a recovery and provide a protection from GBV-C/HGV infection. Whether there is any other recovery marker in serum requires further study.

Objective: Our objective is to study the pathogenicity of the single HGV infection., Methods: The ELISA was used to check the serum anti-HGV antibody of 36 cases. Immunohistochemistry staining of hepatic tissue was conducted by using HGV NS5 McAb in 20 single HGV infected patients who were further confirmed by clinical diagnosis and pathological evidence. These patients included 10 cases of acute hepatitis, 7 cases of chronic hepatitis, 1 cases of subacute severe hepatitis and 2 cases of chronic severe hepatitis., Results: (1) Clinical manifestation: Acute hepatitis occurred abruptly, accompanied with fever, inertia, nausea and sometimes with vomiting and oil disgust. Chronic hepatitis developed slowly and presented mild symptoms. Severe hepatitis presented an acute onset, extreme fatigue, serious gastrointestinal symptoms, or even hepatic coma developed. (2) Changes of ALT and AST: ALT and AST increased slightly in chronic hepatitis and moderately in acute and severe hepatitis. The disproportion between ALT and BiL sometimes occurred in severe hepatitis. (3) Pathological changes in hepatic tissue: Acute hepatitis was characterized by hepatocyte swelling and inflammatory cells infiltrated in portal duct areas. Chronic hepatitis was identified by hepatocyte swelling, piecemeal necrosis or spotty necrosis, slight infiltration of inflammatory cell in portal duct areas and fibrosis. Severe hepatitis appeared as hepatic cell necrosis, inflammatory cell infiltration and slight fibrosis., Conclusions: Infection of HGV can give rise to acute hepatitis, chronic hepatitis and severe hepatitis.

Objective: To study the clinical, enzymatic and liver pathological changes in patients with hepatitis G virus (HGV) infection., Methods: RT- nested PCR was applied to detect HGV RNA in 368 patients with hepatic diseases. The liver biopsy tissue from one liver cirrhosis patient with simple HGV infection was examined., Results: Simple HGV RNA positive were found in 7 cases of 71 acute hepatitis jaundice, in 22 cases of 155 chronic hepatitis and in 3 cases of 51 liver cirrhosis. The immunohistochemistry of the liver biopsy tissue from a liver cirrhosis patient showed HGV NS5 antigen positive. However, HGV infection might occur simply or in combination with hepatitis B or C virus or super infected., Conclusions: HGV RNA could be detected in acute hepatitis jaundice, chronic hepatitis, hepatitis B or C carriers, liver cirrhosis and hepatocellular carcinoma. HGV is proved to be a hepatotropic virus by pathological examination and immunohistochemistry, the virus located in the cytoplasm of the liver cells. It may cause chronic hepatitis and even liver cirrhosis, so HGV is pathogenic to liver tissue.

Objective: To study the infection due to hepatitis G virus (HGV) in liver tissues of patients with acute hepatitis and to investigate its pathogenicity., Methods: HGV NS5 antigen was detected by using immunohistochemical method in the liver biopsy tissues of patients with acute hepatitis but serologically negative to hepatitis virus antigens from A to E. The clinical and pathological data were also analysed., Results: 37 samples were tested, HGV NS5 antigen was detected in 14 (37.8%). 4 of the 14 were positive for HGV NS5 antigen alone (acute hepatitis G group) and 10 other cases were also positive for HBsAg, hepatitis C virus (HCV) NS3 antigen or EB virus antigen (superinfection group). 7 cases were HBsAg positive alone (acute hepatitis B group) and the remaining 16 cases were negative for all the antigens mentioned above (non-A - G hepatitis group). There was no difference among the 4 groups in the detecting rate of Fas antigen, histological activity index (HAI), serum alanine transferase (ALT) and total bilirubin (TBil)., Conclusion: It is suggested that HGV appears to play some role in the pathogenesis of acute viral hepatitis and the degree of liver injury in acute hepatitis G may be as severe as that of hepatitis caused by other types of viruses.

Objective: To study the genesis, development and pathogenesis of hepatitis G., Methods: The Chinese Rhesus monkeys were intravenously injected with the serum from a hepatitis G patient only with HGV RNA positive. The dynamic changes of serum and liver tissues of the animals were observed before and after infection. Also the immunohistochemical study were done with monocolonal antibody against NS5 gene antigen of HGV. One male monkey was dissected and the internal organs were taken for histological examination 18 months after infection., Results: Serum ALT and AST became increasing 30 days after infection and showed abnormal continuously for 9 months. Spotty and focal necrosis and piecemeal necrosis were found in liver tissue from 2 to 18 months after infection. Positive staining of HGV antigen was present in cytoplasm of liver cells by immunohistochemistry. Histological observation showed that the internal organs were normal except the liver tissue in which the damages were similar with that in hepatitis., Conclusion: The successful infection of Chinese Rhesus monkey by serum from hepatitis G patient can used as a good animal model for the study of hepatitis G.